Maternal Stress Experience Research Articles

Understanding working mothers’ difficulty: From need frustration to family–work conflict

Abstract Previous research has primarily focused on the impact of basic psychological needs frustration on parenting styles and its effect on children. However, there is a lack of research on the impact of basic psychological needs frustration in mothers, particularly those who work full time. To fill the gap, this study explores how frustration of needs experienced by full-time working mothers in the family context relates to their experience of maternal stress and family-to-work conflict and the moderating role of financial motivation to work. In a three-wave study of 168 full-time working mothers, we discovered a positive correlation between basic psychological needs frustration and maternal stress, which in turn led to family-to-work conflict. These relationships were more pronounced among mothers with lower financial motivation to work, as opposed to those with higher. We conclude by discussing the implications of our research and suggesting areas for future study.

Transgenerational stress memory in plants is mediated by upregulation of the antioxidative system

Transgenerational stress memory transferred from parents to offspring may enable plants to respond to changing environments rapidly. Yet transgenerational adaptive effects and underlying mechanisms in response to waterlogging and drought are still unclear. Furthermore, transgenerational cross-stress tolerance, pre-adapting offspring to any stress when maternal plants experienced stress, is currently understudied. We conducted a full-factorial pot experiment over two generations, using four perennial plant species and subjecting maternal and offspring plants to waterlogging and drought. We hypothesized that offspring experiencing stress performed better when mothers had experienced stress before, irrespective of the type of stress. We found increased biomass and reproductive output in offspring experiencing the same stress conditions as their mothers (transgenerational adaptive effects). However, a maternal stress experience per se did not pre-condition offspring to other types of stress. Transgenerational adaptive effects were linked to changes in the antioxidative system of one species, reducing oxidative damage through upregulation of protective enzymes in offspring experiencing the same conditions as their mothers. Our research provides evidence for transgenerational waterlogging and drought memory and links this to underlying photosynthetic and redox-related mechanisms. Transgenerational adaptive effects acting on the antioxidative system might therefore contribute to the rapid responses of plants to environmental change.

Maternal Stress Experience in the Neonatal Intensive Care Unit after Preterm Delivery.

Preterm delivery with the admission of a child in the neonatal intensive care unit (NICU) is extremely challenging for parents. Being separated from the baby and seeing her infant feeling pain and being sick together with the complexity of the NICU environment, the mother experiences great anxiety, fear, and stress. The purpose of the study was to assess NICU-related stress and to identify maternal and infant factors associated with increased stress in mothers of preterm infants. The maternal stress level was assessed in 122 mothers of preterm infants using the Parental Stressor Scale: NICU (PSS: NICU) in which items were distributed in three subscales as follows: Sights and Sounds of NICU-subscale 1 (S1), Infant Appearance and Behavior-S2, and Parental Role Alteration-S3. Maternal total PSS: NICU score was 3.46 ± 0.71. Parenteral Role Alteration was the most stressful (4.20 ± 0.79) followed by Infant Appearance and Behavior (3.51 ± 0.91) and Sights and Sounds subscale (2.28 ± 0.95); p (S1-S2) < 0.001, p (S1-S3) < 0.001, and p (S2-S3) < 0.001. Total PSS: NICU and Infant Appearance and Behavior scores correlated positively with maternal age (r = 0.189; p = 0.040 and r = 0.204; p = 0.027, respectively) and duration of NICU treatment (r = 0.188; p = 0.044 and r = 0.190; p = 0.042). More visits in NICU by a mother were associated with a lower PSS: NICU score (p = 0.049) and neonatal seizures and invasive ventilation in infants were associated with higher stress scores (p = 0.007 and p = 0.042). Mothers of preterm infants admitted in the NICU experience significant stress which is correlated with maternal age and NICU treatment duration and is associated with frequency of NICU visits, presence of neonatal seizures, and need for ventilator support. Parental role alteration is the greatest stressor followed by Infant Appearance and Behavior and NICU-surrounding stressor factors which show the need for interventions and counseling focused on mothers' role, their involvement in infant's care, and thus, family-centered care implementation. · Mothers of preterm infants experience significant stress.. · Parental role alteration is the greatest maternal stressor.. · Maternal stress is correlated with age and NICU duration, and is associated with the frequency of NICU visits and infant's health status.

356 Microbial origins in the developmental programming of offspring health

Abstract Adverse parental lifetime experiences, such as stress and malnutrition, are implicated in the risk for offspring metabolic, cardiovascular, and neurodevelopmental disorders. In recent years, the maternal microbiome has emerged as an important factor that affects maternal health and infant development during pregnancy and beyond. Using mouse models of maternal stress experience during pregnancy, we examined the hypothesis that maternal stress experience alters the composition of the maternal microbiota and this altered community is transmitted to offspring to mediate effects of prenatal stress. As maternal stress exposure exhibits disruptive effects on both in utero environment and maternal microbiota, it has been difficult to assess the mechanistic involvement of the maternal microbiome to the prenatal stress phenotype independent of stress effects on the fetal environment. To circumvent this, we developed a maternal microbiota transplantation method in which embryonic day 18.5 mouse pups were delivered by caesarean section, thereby preventing natural colonization, and then transplanted with various maternal microbiota communities via orogastric gavage. Transplantation of maternal microbiota from stressed dams into naïve pups delivered by caesarean section recapitulated phenotypes that resembled those seen in prenatally stressed males, including reduced body weight and increased neuroendocrine response to acute stressors. However, transplantation of control maternal vaginal microbiota into prenatally stressed pups delivered by caesarean section did not rescue the prenatal stress phenotype. We showed that the inability to rescue the prenatal stress phenotype is related to transcriptional reprogramming to pathways involved in the regulation of innate immunity in the fetal gut and brain prior to birth and colonization by maternal microbiota. These results are interesting in light of recent studies demonstrating a critical role of the maternal microbiome on homeostasis of immune cell populations in the offspring brain. As an important requirement for normal growth and development, metabolites produced by the maternal gut microbiota cross the placental barrier and gain access to fetal circulation. Thus, we examined the hypothesis that maternal stress experience during pregnancy significantly alters the availability of maternal gut microbiota-derived metabolites, thereby shifting the availability of these metabolites required for the developing brain. Metabolomic profiling of the maternal compartment and fetal brain showed stress-induced reduction in a class of microbiota-derived metabolites involved in immune homeostasis and chromatin remodeling. Indeed, functional profiling of immune populations in the fetal brain revealed an association between reduced metabolite availability and increased infiltration of proinflammatory monocytes in the fetal brain. Further, as the gut microbiome is fairly accessible within clinical settings, we are now also asking how our mouse model translates to humans in a cohort of pregnant women exposed to childhood adversity. Collectively, our results suggest that intergenerational transmission of stress exposure occur via the maternal microbiota through two novel mechanisms. First, stress alterations during pregnancy impact the available pool of maternal gut microbiota-derived metabolites necessary for normal prenatal growth and development. Second, transmission of stress-altered vaginal microbiota may alter critical immune and metabolic processes underlying neurodevelopment.

The relationship between maternal stress during pregnancy and up to two years after birth and risk of child overweight and obesity: Protocol for a Systematic Review

Background: Childhood obesity presents a significant public health challenge globally. The period from conception to two years after birth, the first 1000 days, represents a critical period during which the experience of maternal stress may be related to the development of childhood obesity. Research to date suggests some positive associations between maternal stress during the first 1000 days and childhood obesity, but findings are inconsistent and have not yet been comprehensively synthesised. The purpose of this review is to systematically examine the association between maternal stress during the first 1000 days and the risk of child overweight and obesity. Methods: The following electronic databases will be searched from inception using a detailed search strategy: the Cochrane Library, MEDLINE, PsycINFO, EMBASE, CINAHL, Maternity and Infant Care, and Web of Science. Cohort, case-control, and cross-sectional studies examining maternal stress during the first 1000 days and child overweight and obesity up to the age of 10 years will be included. Titles, abstracts and full articles will be screened by two investigators independently to identify eligible studies. A standardised data extraction form will be used to extract data including: study design; maternal stress exposure; child outcome; exclusion criteria; participant characteristics; and assessment methods. The Cochrane Collaboration’s bias classification tool for observational studies will be used to assess study quality. This protocol is reported according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses protocol (PRISMA-P) checklist, and the systematic review will be conducted and reported following the PRISMA checklist. If possible, random effects models will be used to perform meta-analyses. Ethics and dissemination: Ethical approval is not required for this study as it will not involve conducting experimental research, nor include identifying personal data. The systematic review will be disseminated in peer-reviewed journals. PROSPERO registration number: CRD42018100363

Larger Amygdala Volume Mediates the Association Between Prenatal Maternal Stress and Higher Levels of Externalizing Behaviors: Sex Specific Effects in Project Ice Storm.

Introduction: The amygdala is a brain structure involved in emotional regulation. Studies have shown that larger amygdala volumes are associated with behavioral disorders. Prenatal maternal depression is associated with structural changes in the amygdala, which in turn, is predictive of an increase in behavioral problems. Girls may be particularly vulnerable. However, it is not known whether disaster-related prenatal maternal stress (PNMS), or which aspect of the maternal stress experience (i.e., objective hardship, subjective distress, and cognitive appraisal), influences amygdala volumes. Nor is it known whether amygdala volumes mediate the effect of PNMS on behavioral problems in girls and boys.Aims: To assess whether aspects of PNMS are associated with amygdala volume, to determine whether timing of exposure moderates the effect, and to test whether amygdala volume mediates the association between PNMS and internalizing and externalizing problems in 11½ year old children exposed in utero, to varying levels of disaster-related PNMS.Methods: Bilateral amygdala volumes (AGV) and total brain volume (TBV) were acquired using magnetic resonance imaging, from 35 boys and 33 girls whose mothers were pregnant during the January 1998 Quebec Ice Storm. The mothers' disaster-related stress was assessed in June 1998. Child internalizing and externalizing problems were assessed at 11½ years using the Child Behavior Checklist (CBCL). Hierarchical regression analyses and mediation analyses were conducted on boys and girls separately, controlling for perinatal and postnatal factors.Results: In boys, subjective distress was associated with larger right AGV/TBV when mothers where exposed during late pregnancy, which in turn explained higher levels of externalizing behavior. However, when adjusting for postnatal factors, the effect was no longer significant. In girls, later gestational exposure to the ice storm was associated with larger AGV/TBV, but here, higher levels of objective PNMS were associated with more externalizing problems, which was, in part, mediated by larger AGV/TBV. No effects were detected on internalizing behaviors.Conclusion: These results suggest that the effects of PNMS on amygdala development and externalizing symptoms, as assessed in boys and girls in early adolescence, can be influenced by the timing of the stress in pregnancy, and the particular aspect of the mother's stress experience.

38. Stress Alterations to the Maternal Microbiome Mediate Sex-Specific Neuroimmune Development

Maternal stress experience during pregnancy produces lasting effects on the developing brain, increasing subsequent risk for neuropsychiatric disorders throughout life. Using our well-established mouse model of early prenatal stress, in which exposed males exhibit lasting reprogramming of hypothalamic circuits controlling neuroendocrine response to stress and metabolism. As newborns acquire the initial community of microbiota from the mother during birth, we transplanted vaginal microbiota from stressed dams into naïve pups delivered by cesarean section and recapitulated key aspects of the prenatal stress phenotype. However, the inability to rescue the prenatal stress phenotype involved transcriptional reprogramming to innate immunity pathways in the fetal gut and brain. Thus, we examined the hypothesis that sex-specific neuroimmune development is influenced by stress effects on the maternal gut microbiome.

Effects of maternal stress during pregnancy and up to two years after birth on risk of child overweight and obesity: Protocol for a Systematic Review

Background: Childhood obesity presents a significant public health challenge globally. The period from conception to two years after birth, the first 1000 days, represents a critical period during which the experience of maternal stress may be related to the development of childhood obesity. Research to date suggests some positive associations between maternal stress during the first 1000 days and childhood obesity, but findings are inconsistent and have not yet been comprehensively synthesised. The purpose of this review is to systematically examine the association between maternal stress during the first 1000 days and the risk of child overweight and obesity. Methods: The following electronic databases will be searched from inception using a detailed search strategy: the Cochrane Library, MEDLINE, PsycINFO, EMBASE, CINAHL, Maternity and Infant Care, and Web of Science. Cohort, case-control, and cross-sectional studies examining maternal stress during the first 1000 days and child overweight and obesity up to the age of 10 years will be included. Titles, abstracts and full articles will be screened by two investigators independently to identify eligible studies. A standardised data extraction form will be used to extract data including: study design; maternal stress exposure; child outcome; exclusion criteria; participant characteristics; and assessment methods. The Cochrane Collaboration’s bias classification tool for observational studies will be used to assess study quality. This protocol is reported according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses protocol (PRISMA-P) checklist, and the systematic review will be conducted and reported following the PRISMA checklist. If possible, random effects models will be used to perform meta-analyses. Ethics and dissemination: Ethical approval is not required for this study as it will not involve conducting experimental research, nor include identifying personal data. The systematic review will be disseminated in peer-reviewed journals. PROSPERO registration number: CRD42018100363

Effects of maternal stress during pregnancy and up to two years after birth on risk of child overweight and obesity: Protocol for a Systematic Review

Background: Childhood obesity presents a significant public health challenge globally. The period from conception to two years after birth, the first 1000 days, represents a critical period during which the experience of maternal stress may be related to the development of childhood obesity. Research to date suggests some positive associations between maternal stress during the first 1000 days and childhood obesity, but findings are inconsistent and have not yet been comprehensively synthesised. The purpose of this review is to systematically examine the association between maternal stress during the first 1000 days and the risk of child overweight and obesity. Methods: The following electronic databases will be searched from inception using a detailed search strategy: the Cochrane Library, MEDLINE, PsycINFO, EMBASE, CINAHL, Maternity and Infant Care, and Web of Science. Cohort, case-control, and cross-sectional studies examining maternal stress during the first 1000 days and child overweight and obesity up to the age of 12 years will be included. Titles, abstracts and full articles will be screened by two investigators independently to identify eligible studies. A standardised data extraction form will be used to extract data including: study design; maternal stress exposure; child outcome; exclusion criteria; participant characteristics; and assessment methods. The Cochrane Collaboration’s bias classification tool for observational studies will be used to assess study quality. This protocol is reported according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses protocol (PRISMA-P) checklist, and the systematic review will be conducted and reported following the PRISMA checklist. If possible, random effects models will be used to perform meta-analyses. Ethics and dissemination: Ethical approval is not required for this study as it will not involve conducting experimental research, nor include identifying personal data. The systematic review will be disseminated in peer-reviewed journals. PROSPERO registration number: CRD42018100363

Prenatal Immune and Endocrine Modulators of Offspring's Brain Development and Cognitive Functions Later in Life.

Milestones of brain development in mammals are completed before birth, which provide the prerequisite for cognitive and intellectual performances of the offspring. Prenatal challenges, such as maternal stress experience or infections, have been linked to impaired cognitive development, poor intellectual performances as well as neurodevelopmental and psychiatric disorders in the offspring later in life. Fetal microglial cells may be the target of such challenges and could be functionally modified by maternal markers. Maternal markers can cross the placenta and reach the fetus, a phenomenon commonly referred to as “vertical transfer.” These maternal markers include hormones, such as glucocorticoids, and also maternal immune cells and cytokines, all of which can be altered in response to prenatal challenges. Whilst it is difficult to discriminate between the maternal or fetal origin of glucocorticoids and cytokines in the offspring, immune cells of maternal origin—although low in frequency—can be clearly set apart from offspring's cells in the fetal and adult brain. To date, insights into the functional role of these cells are limited, but it is emergingly recognized that these maternal microchimeric cells may affect fetal brain development, as well as post-natal cognitive performances and behavior. Moreover, the inheritance of vertically transferred cells across generations has been proposed, yielding to the presence of a microchiome in individuals. Hence, it will be one of the scientific challenges in the field of neuroimmunology to identify the functional role of maternal microchimeric cells as well as the brain microchiome. Maternal microchimeric cells, along with hormones and cytokines, may induce epigenetic changes in the fetal brain. Recent data underpin that brain development in response to prenatal stress challenges can be altered across several generations, independent of a genetic predisposition, supporting an epigenetic inheritance. We here discuss how fetal brain development and offspring's cognitive functions later in life is modulated in the turnstile of prenatal challenges by introducing novel and recently emerging pathway, involving maternal hormones and immune markers.

Long-Term Sex-Dependent Vulnerability to Metabolic challenges in Prenatally Stressed Rats.

Prenatal stress (PNS) might affect the developmental programming of adult chronic diseases such as metabolic and mood disorders. The molecular mechanisms underlying such regulations may rely upon long-term changes in stress-responsive effectors such as Brain-Derived Neurotrophic Factor (BDNF) that can affect neuronal plasticity underlying mood disorders and may also play a role in metabolic regulation. Based upon previous data, we hypothesized that PNS might lead to greater vulnerability to an obesogenic challenge experienced at adulthood. In order to investigate our hypothesis, pregnant Sprague-Dawley female rats underwent a chronic procedure of restraint stress during the last week of gestation. The adult offspring were then challenged with a high fat diet (HFD) over 8 weeks and tested for metabolic and emotional endpoints. Moreover, brain specific changes in Bdnf expression levels were also assessed. Overall, HFD resulted in increased caloric intake, insulin resistance, impaired glucose tolerance and higher circulating levels of leptin, while PNS increased the leptin/adiponectin ratio, an index of metabolic risk in adult male subjects. Interestingly, HFD consumption increased anxiety-like behaviors in the Elevated Plus Maze, particularly in males, and this effect was buffered by PNS. Levels of Bdnf were finely modulated by PNS and HFD in a region- and sex-dependent fashion: female offspring overall showed greater plasticity, possibly mediated through increased total Bdnf mRNA expression both in the hippocampus and in the hypothalamus. In conclusion, while the experience of maternal stress during intrauterine life promotes metabolic dysfunction induced by a HFD at adulthood, the interaction between PNS and HFD is positive in male subjects, and in agreement with the match-mismatch hypothesis, resulting in a reduction of anxious behaviors.

Stress during pregnancy alters temporal and spatial dynamics of the maternal and offspring microbiome in a sex-specific manner

The microbiome is a regulator of host immunity, metabolism, neurodevelopment, and behavior. During early life, bacterial communities within maternal gut and vaginal compartments can have an impact on directing these processes. Maternal stress experience during pregnancy may impact offspring development by altering the temporal and spatial dynamics of the maternal microbiome during pregnancy. To examine the hypothesis that maternal stress disrupts gut and vaginal microbial dynamics during critical prenatal and postnatal windows, we used high-resolution 16S rRNA marker gene sequencing to examine outcomes in our mouse model of early prenatal stress. Consistent with predictions, maternal fecal communities shift across pregnancy, a process that is disrupted by stress. Vaginal bacterial community structure and composition exhibit lasting disruption following stress exposure. Comparison of maternal and offspring microbiota revealed that similarities in bacterial community composition was predicted by a complex interaction between maternal body niche and offspring age and sex. Importantly, early prenatal stress influenced offspring bacterial community assembly in a temporal and sex-specific manner. Taken together, our results demonstrate that early prenatal stress may influence offspring development through converging modifications to gut microbial composition during pregnancy and transmission of dysbiotic vaginal microbiome at birth.

Sleep Problems in Young Children with Autism Spectrum Disorders: A Study of Parenting Stress, Mothers' Sleep-Related Cognitions, and Bedtime Behaviors.

Disrupted sleep is common among children with autism spectrum disorder (ASD). Our goal was to (1) examine the contribution of sleep problems to parenting stress in children with ASD as compared to typically developing (TD) and (2) to address maternal sleep-related cognitions and behaviors in both groups. Mothers of 34 ASD (mean age = 39.29 months, SD = 5.22) and 31 TD children (mean age = 36.23 months, SD = 5.75) completed questionnaires measuring maternal stress, sleep-related cognitions and settling to sleep interactions, and the child's sleep problems; mothers in the ASD group completed a symptom severity questionnaire. In accord with previous research, children with ASD had more sleep problems compared to the TD group, and their mothers reported higher levels of stress. In the ASD group, sleep problems contributed to the experience of maternal stress, over and above symptom severity. Across groups, maternal cognitions and bedtime interactions were significantly associated with children's sleep problems. The results highlight the interplay between sleep-related cognitions, bedtime interactions, and sleep problems and underscore the contribution of disrupted sleep to mothers' experience of parenting stress. As sleep problems in ASD children are common, clinicians are advised to include sleep in consultations with parents.

Effect of Maternal Stress Prior to Conception on Hippocampal BDNF Signaling in Rat Offspring.

Environmental factors, especially stress, can remain pervasive effects across the lifespan. Traumatic experiences are risk factors for the behavioral and emotional disorders. Since brain-derived neurotrophic factor (BDNF) is the important regulator of neural survival, development, and its genetic and epigenetic alterations which have been linked with several neuropsychiatric disorders, the present study investigated the effect of maternal adulthood stress on molecular changes of BDNF and tyrosine kinase-coupled receptor (TrkB) in the hippocampus of 30-day-old offspring. To induce stress, we employed a repeated forced swimming model for female rats across 21days. Then, they were divided into two parental breeding groups: stressed mother (SM) and non-stressed mother (NSM) or control group. Anxiety-like behavior was tested in adult female rats and 30-day-old pups by using the elevated plus maze (EPM). The level of serum corticosterone was also measured by ELISA. BDNF and TrkB gene methylation and protein expression in the hippocampus were detected using real-time PCR and Western blotting in all groups. Thirty-day-old male and female pups from SM groups had a significantly more serum corticosterone concentration, DNA methylation levels of BDNF and TrKB, and lower expression of these genes compared to pups from the control groups. Also, male pups from stressed mother exhibited significant anxiety-like behavior compared to male pups from the control mothers. These findings suggest that molecular changes formed by maternal stress experience even before conception persist to the next generation and will negatively influence on phenotypes of offspring.

Parent–Child Groups for Externalizing Disorders: Outcomes, Sociodemographic Moderators, Attendance, and Attrition in a Real-World Setting

ABSTRACTGroup-based parent training is a well-established, empirically supported treatment for externalizing problems, but few studies have examined the outcomes of this approach in real-world, clinically representative outpatient samples. In addition, many families experience barriers to program attendance in outpatient settings. The purpose of this study was to examine pretreatment to posttreatment clinical outcomes of parent training and child social skills groups, as well as sociodemographic moderators of group outcomes, attendance, and attrition, among a large, diverse sample of families attending 8-week group treatment at an outpatient pediatric hospital. Two hundred thirty-three children ages 4–10 years and their parent reporters participated in 28 concurrent parent–child groups. Parent pretreatment and posttreatment ratings of child disruptive behavior and related parental stress were available for 158 families (M child age = 7.25 years, SD = 1.54; 77.8% male). Children showed significant pretreatment to posttreatment reductions in parent-reported child behavior problems and related stress, with small to medium effect sizes. Results showed little variation by sociodemographic moderators. Pretreatment maternal stress experience was associated with retention in treatment among families with both mother and father reporters attending treatment sessions, whereas across all mother reporters a higher degree of pretreatment child-related stress was associated with increased likelihood of group attrition. Medicaid insurance status was associated with increased likelihood of attrition across the full sample of families. The clinical implications of these results and related practice points for enhancing implementation of and patient retention in outpatient parent–child groups are discussed.

Ethnic discrimination predicts poor self-rated health and cortisol in pregnancy: Insights from New Zealand

Despite growing research emphasis on understanding the health effects of ethnic discrimination, little work has focused on how such exposures may influence a woman's biology and health during pregnancy. Understanding such effects is important given evidence that maternal stress experience in pregnancy can have long term effects on offspring health. Here we present data evaluating the relationship between perceived discrimination, self-rated health, and the stress hormone cortisol measured in late pregnancy among a diverse sample of women living in Auckland, New Zealand (N = 55). We also evaluated possible intergenerational impacts of maternal discrimination on stress reactivity in a subset of offspring (N = 19). Pregnant women were recruited from two antenatal care clinics in Auckland. Women were met in their homes between 34 and 36 weeks gestation, during which time a prenatal stress questionnaire was administered and saliva samples (morning and evening from two days) were obtained. Offspring cortisol reactivity was assessed at the standard six week postnatal vaccination visit. We found that 34% of women reported having experienced ethnic discrimination, with minority and immigrant women being more likely to report being angry or upset in response to discrimination experience compared with NZ-born women of European descent. Women reporting discrimination experience had worse self-rated health, higher evening cortisol and gave birth to infants with higher cortisol reactivity, all independent of ethnicity and material deprivation. These findings suggest that discrimination experience can have biological impacts in pregnancy and across generations, potentially contributing to the ethnic gradient in health.

Prenatal stress increases the obesogenic effects of a high-fat-sucrose diet in adult rats in a sex-specific manner

Stress during pregnancy can induce metabolic disorders in adult offspring. To analyze the possible differential response to a high-fat-sucrose (HFS) diet in offspring affected by prenatal stress (PNS) or not, pregnant Wistar rats (n = 11) were exposed to a chronic mild stress during the third week of gestation. The aim of this study was to model a chronic depressive-like state that develops over time in response to exposure of rats to a series of mild and unpredictable stressors. Control dams (n = 11) remained undisturbed. Adult offspring were fed chow or HFS diet (20% protein, 35% carbohydrate, 45% fat) for 10 weeks. Changes in adiposity, biochemical profile, and retroperitoneal adipose tissue gene expression by real-time polymerase chain reaction were analyzed. An interaction was observed between HFS and PNS concerning visceral adiposity, with higher fat mass in HFS-fed stressed rats, statistically significant only in females. HFS modified lipid profile and increased insulin resistance biomarkers, while PNS reduced insulin concentrations and the homeostasis model assessment index. HFS diet increased gene (mRNA) expression for leptin and apelin and decreased cyclin-dependent kinase inhibitor 1A and fatty acid synthase (Fasn), whereas PNS increased Fasn and stearoyl-CoA desaturase1. An interaction between diet and PNS was observed for adiponutrin (Adpn) and peroxisome proliferator-activated receptor-γ coactivator1-α (Ppargc1a) gene expression: Adpn was increased by the PNS only in HFS-fed rats, whereas Ppargc1a was increased by the PNS only in chow-fed rats. From these results, it can be concluded that experience of maternal stress during intrauterine development can enhance predisposition to obesity induced by a HFS diet intake.

Sex differences in prenatal epigenetic programing of stress pathways

Maternal stress experience is associated with neurodevelopmental disorders including schizophrenia and autism. Recent studies have examined mechanisms by which changes in the maternal milieu may be transmitted to the developing embryo and potentially translated into programing of the epigenome. Animal models of prenatal stress have identified important sex- and temporal-specific effects on offspring stress responsivity. As dysregulation of stress pathways is a common feature in most neuropsychiatric diseases, molecular and epigenetic analyses at the maternal–embryo interface, especially in the placenta, may provide unique insight into identifying much-needed predictive biomarkers. In addition, as most neurodevelopmental disorders present with a sex bias, examination of sex differences in the inheritance of phenotypic outcomes may pinpoint gene targets and specific windows of vulnerability in neurodevelopment, which have been disrupted. This review discusses the association and possible contributing mechanisms of prenatal stress in programing offspring stress pathway dysregulation and the importance of sex.